PM2.5-induced inflammation and lipidome alteration associated with the development of atherosclerosis based on a targeted lipidomic analysis

Jingyi Zhang; Shuang Liang; Ruihong Ning; Jinjin Jiang; Jie Zhang; Heqing Shen; Rui Chen; Junchao Duan; Zhiwei Sun

Environment International (Mar 2020)

PM2.5-induced inflammation and lipidome alteration associated with the development of atherosclerosis based on a targeted lipidomic analysis

Jingyi Zhang,
Shuang Liang,
Ruihong Ning,
Jinjin Jiang,
Jie Zhang,
Heqing Shen,
Rui Chen,
Junchao Duan,
Zhiwei Sun

Affiliations

Jingyi Zhang: Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China
Shuang Liang: Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China
Ruihong Ning: Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China
Jinjin Jiang: Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China
Jie Zhang: State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen 361102, PR China
Heqing Shen: State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen 361102, PR China; Key Laboratory of Urban Environment and Health, Institute of Urban Environment, Chinese Academy of Sciences, Xiamen 361021, PR China
Rui Chen: Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China
Junchao Duan: Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China; Corresponding authors at: School of Public Health, Capital Medical University, Beijing 100069, PR China.
Zhiwei Sun: Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China; Corresponding authors at: School of Public Health, Capital Medical University, Beijing 100069, PR China.

Journal volume & issue: Vol. 136

Abstract

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Epidemiological studies have confirmed that PM2.5 could contribute to the development of atherosclerosis accompanied with lipids dysregulation. However, the lipids biomarkers involved in this progress remain largely unknown. In this study, a targeted lipidomic approach was used to find out the possible lipid biomarkers involved in the development of atherosclerosis after PM2.5 exposure or during a recovery period. Also, we assessed the pro-atherosclerosis effects of PM2.5 and follow-up influence using pulse wave (PW) Doppler ultrasound, oil red O staining and H&E staining. The vascular stiffness was elevated after 2-month PM2.5 exposure and might persist after 1-month recovery. While the lesions mostly concentrated in the aortic arch was significantly increased in 2-month PM2.5 exposure group and remained an increasing trend after 1-month recovery. The expressions of pro-inflammatory cytokines detected by Mouse Inflammation Array were elevated after ApoE−/− mice treated with PM2.5 for 2-month and restored following 1-month recovery. Yet, IL-10 was significantly decreased during 1-month recovery. Additionally, the targeted lipidomic analysis demonstrated that cholesterol ester (CE), phosphatidylcholine (PC), phosphatidylethanolamine (PE), sphingomyelin (SM) were significantly increased while lysophosphatidylethanolamine (LPE), lysophosphatidylcholine (LPC), diacylglycerol (DG), triacylglycerol (TG) were reduced after 2-month PM2.5 exposure, indicating that PM2.5 could disrupt glycerophospholipids, glycerolipids and sphingolipids metabolism. And a persistent impact of PM2.5 on glycerophospholipids and glycerolipids metabolism was found after 1-month recovery. Our study demonstrated that PM2.5-induced inflammation response might promote atherosclerotic lesions probably through lipid dysregulation, and the influence probably persisted after 1-month recovery. Keywords: PM2.5, Atherosclerosis, Inflammation, Lipidomic, Glycerophospholipids, Glycerolipids

Published in Environment International

ISSN: 0160-4120 (Print)
Publisher: Elsevier
Country of publisher: United Kingdom
LCC subjects: Geography. Anthropology. Recreation: Environmental sciences
Website: https://www.journals.elsevier.com/environment-international

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